细胞凋亡与小鼠病毒性心肌炎的实验研究

目的 :探讨细胞凋亡在病毒性心肌炎发病中的作用。方法 :采用光镜、电镜、原位末端标记法 (TUNEL)观察病毒性心肌炎 (viralmyocarditis ,VM)鼠不同时期病理改变及细胞凋亡情况。结果 :小鼠感染后 7d即见炎性细胞浸润及心肌坏死 ,10～ 14d病变最严重 ,2 1d以后心肌炎性细胞浸润及心肌坏死逐渐减轻 ,代之心肌纤维化 ,对照组无病变。实验组 7、10、14、2 1、2 8d均可见到凋亡细胞 ,且感染后 7～ 14d细胞凋亡数明显高于 2 1～ 2 8d(P <0 .0 5 ) ,对照组未见凋亡细胞。结论 :细胞凋亡在病毒性心肌炎中起着重要作用 ,它参与了病毒性心肌炎的发生、发展。

The Experimental Research on Apoptosis and Virus Myocarditis in Mice

Objective To investigate the role of apoptosis in the development of virus myocarditis in mice. Methods Light microscopy, electyonic microscopy and terminal transferase-mediated dUTP-biotin nick end-labeling(TUNEL)assays were used to detect the inflammtion, necrosis and apoptosis in myocardium. Results (1)The typical myocardial lesions including myocardial necrosis and lymphocyte infiltration at the 7 th day post-inoculation were observed, with much worse results between the 10th and 14th day, and recovered from the 21th to 28th day, and without any inflammtion in control group. (2)TUNEL-positive myocytes appeared in the myocardium of myocarditis mice on days 7,10,14,21,28. The percent of apoptosis myocytes were much higher 7 to 14 days after the infection than 21 to 28 days(P<0.05).The mice in control group did not have any apoptosis cell. Conclusion Apoptosis playS an important role in the virus myocarditis. It is involved in the pathogenesis of virus myocarditis in mice.